Traumatic subarachnoid haemorrhage: a 10-year case study and review

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Abstract

Fourteen cases of traumatic subarachnoid haemorrhage (TSAH) from the years 1985–1995 are described. Two of these cases, one paediatric and one involving controlled substances, are considered separately. All 14 cases are then discussed together with the current literature with respect to: typical subject, the circumstances and aetiology of injury, time interval between injury and collapse, time of survival, the role of alcohol, the site of arterial rupture, and the methods recommended by other authors for the location of such an injury. We conclude that TSAH is a poorly understood cause of sudden death; fuller research is needed to clarify aetiology.

Introduction

In 1994 Leadbeatter [1] called into question the existence of what was previously a widely accepted cause of sudden death; massive basal subarachnoid haemorrhage as a direct result of trauma. This pathological entity has been recognised since Ford [3] described a series in 1956 and, even earlier, Wilks [2] suggested a relationship between trauma and subarachnoid haemorrhage in the nineteenth century.

This type of haemorrhage is typically associated with injury to the neck, although occasionally it may follow unrestricted movement of the head upon the neck. The trauma may be inflicted by a blow with the fist or hand, a blunt instrument, or a blow with a shod foot. Less commonly, a blow to the head rather than the neck is the cause, but this is apparently unusual [30].

One difficulty that has been encountered by those in the reporting of cases of this process has been identification of the site of rupture, with careful dissection [4] and angiography [5] being advised for precise visualisation of the defects. Contostavlos [6] noted that the blood does not remain localised in the subarachnoid space around the area of trauma, thus increasing the difficulty in the search for a ruptured vessel. He also stated that a clot provides no evidence of a bleed at a vertebral artery tear site if the entire subarachnoid haemorrhage is clotted. There has been ongoing controversy over the site of injury in these cases, and the technique for its demonstration.

We have identified and studied 14 cases of traumatic basal subarachnoid haemorrhage (TSAH) from the Department of Forensic Pathology, University of Sheffield, archival records for the period 1985–95. From these the exact circumstances of death were determined and post-mortem reports assessed. We discuss our findings in relation to the current literature.

Section snippets

Case reports

The circumstances, survival time, alcohol level, and autopsy findings are illustrated in Table 1. Of these 14, we particularly comment on the findings in cases 12 and 13; the remainder are summarised below.

Of our 14 cases, 11 were male (one of whom was a 2-year-old infant) and three female. The ages ranged from 2 to 53 years (mean, 33 years). In nine cases the site of rupture was positively identified. None of our cases regained consciousness following the initial incident and six died within 1

A typical subject

In 1986 Deck and Jaghada [10] described traumatic subarachnoid haemorrhage as typically occurring in a “young, healthy, but intoxicated man who receives a minor blow, immediately collapses, and dies within minutes.”

Tatsuno and Lindenburg [11] carried out a study on deaths due to this cause in 1973 and found that 85% were men. The youngest person was an 18-year-old man. However, most of the cases were found to occur in the fourth decade. Other work has also supported these observations in a

Conclusions

This review attempts to collate the many observations and disparate theories of causation advanced by previous workers, particularly in light of Leadbeatter’s controversial views. However, it has proved impossible to reach any firm conclusions.

The causes of TSAH, and the possibility of direct brainstem/spinal cord trauma, must remain conjectural. We believe that TSAH is an important cause of death in adults, even when the related neck or head injury is apparently only minor. Furthermore, we are

Acknowledgments

We would like to thank Dr N. Carter and Dr G.N. Rutty for their invaluable assistance. We would also like to thank all other members of staff at The Department of Forensic Pathology, The University of Sheffield.

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